Implant-supported mandibular overdentures and cortical bone formation: clinical and radiographic results

PURPOSE: The aim of this study was to evaluate the hard and soft tissue parameters around implants supporting overdentures and the possible influence of increased periimplant bone density (IPBD) on implant success. MATERIALS AND METHODS: A total of 44 dental implants placed in the mandible of 12 patients were included in the study. Implants were divided in 2 groups in relation to the optically detected IPBD. Periimplant clinical and radiographic variables were collected over the period of 5 years. RESULTS: Periimplant clinical and radiographic parameters for all implants did not change significantly throughout the observation period (P > 0.05). Significant differences were observed between implants with and without IPBD for periimplant soft tissue parameters and Periotest values (P < 0.05). Implants with and without IPBD at 5-year control showed mean bone loss of 0.04 ± 0.48 mm and 0.55 ± 0.96 mm, respectively (P = 0.026). All density values decreased throughout the observation period, except maximal values for implants with IPBD that overcome the initial values at the 5-year control. CONCLUSIONS: Implants supporting overdentures were clinically successful over the period of follow-up. IPBD may be related to the maintenance of the periimplant bone level.

Cortical reorganisation of cerebral networks after childhood stroke: impact on outcome.

BACKGROUND Recovery after arterial ischaemic stroke is known to largely depend on the plastic properties of the brain. The present study examines changes in the network topography of the developing brain after stroke. Effects of brain damage are best assessed by examining entire networks rather than single sites of structural lesions. Relating these changes to post-stroke neuropsychological variables and motor abilities will improve understanding of functional plasticity after stroke. Inclusion of healthy controls will provide additional insight into children's normal brain development. Resting state functional magnetic resonance imaging is a valid approach to topographically investigate the reorganisation of functional networks after a brain lesion. Transcranial magnetic stimulation provides complementary output information. This study will investigate functional reorganisation after paediatric arterial ischaemic stroke by means of resting state functional magnetic resonance imaging and transcranial magnetic stimulation in a cross-sectional plus longitudinal study design. The general aim of this study is to better understand neuroplasticity of the developing brain after stroke in order to develop more efficacious therapy and to improve the post-stroke functional outcome. METHODS The cross-sectional part of the study will investigate the functional cerebral networks of 35 children with chronic arterial ischaemic stroke (time of the lesion >2 years). In the longitudinal part, 15 children with acute arterial ischaemic stroke (shortly after the acute phase of the stroke) will be included and investigations will be performed 3 times within the subsequent 9 months. We will also recruit 50 healthy controls, matched for age and sex. The neuroimaging and neurophysiological data will be correlated with neuropsychological and neurological variables. DISCUSSION This study is the first to combine resting state functional magnetic resonance imaging and transcranial magnetic stimulation in a paediatric population diagnosed with arterial ischaemic stroke. Thus, this study has the potential to uniquely contribute to the understanding of neuronal plasticity in the brains of healthy children and those with acute or chronic brain injury. It is expected that the results will lead to the development of optimal interventions after arterial ischaemic stroke.

Dysfunction of Cortical Dendritic Integration in Neuropathic Pain Reversed by Serotoninergic Neuromodulation

Neuropathic pain is caused by long-term modifications of neuronal function in the peripheral nervous system, the spinal cord, and supraspinal areas. Although functional changes in the forebrain are thought to contribute to the development of persistent pain, their significance and precise subcellular nature remain unexplored. Using somatic and dendritic whole-cell patch-clamp recordings from neurons in the anterior cingulate cortex, we discovered that sciatic nerve injury caused an activity-dependent dysfunction of hyperpolarization-activated cyclic nucleotide-regulated (HCN) channels in the dendrites of layer 5 pyramidal neurons resulting in enhanced integration of excitatory postsynaptic inputs and increased neuronal firing. Specific activation of the serotonin receptor type 7 (5-HT7R) alleviated the lesion-induced pathology by increasing HCN channel function, restoring normal dendritic integration, and reducing mechanical pain hypersensitivity in nerve-injured animals in vivo. Thus, serotoninergic neuromodulation at the forebrain level can reverse the dendritic dysfunction induced by neuropathic pain and may represent a potential therapeutical target.

Methylation of NR3C1 is related to maternal PTSD, parenting stress and maternal medial prefrontal cortical activity in response to child separation among mothers with histories of violence exposure.

Prior research has shown that mothers with Interpersonal violence-related posttraumatic stress disorder (IPV-PTSD) report greater difficulty in parenting their toddlers. Relative to their frequent early exposure to violence and maltreatment, these mothers display dysregulation of their hypothalamic pituitary adrenal axis (HPA-axis), characterized by hypocortisolism. Considering methylation of the promoter region of the glucocorticoid receptor gene NR3C1 as a marker for HPA-axis functioning, with less methylation likely being associated with less circulating cortisol, the present study tested the hypothesis that the degree of methylation of this gene would be negatively correlated with maternal IPV-PTSD severity and parenting stress, and positively correlated with medial prefrontal cortical (mPFC) activity in response to video-stimuli of stressful versus non-stressful mother-child interactions. Following a mental health assessment, 45 mothers and their children (ages 12-42 months) participated in a behavioral protocol involving free-play and laboratory stressors such as mother-child separation. Maternal DNA was extracted from saliva. Interactive behavior was rated on the CARE-Index. During subsequent fMRI scanning, mothers were shown films of free-play and separation drawn from this protocol. Maternal PTSD severity and parenting stress were negatively correlated with the mean percentage of methylation of NR3C1. Maternal mPFC activity in response to video-stimuli of mother-child separation versus play correlated positively to NR3C1 methylation, and negatively to maternal IPV-PTSD and parenting stress. Among interactive behavior variables, child cooperativeness in play was positively correlated with NR3C1 methylation. Thus, the present study is the first published report to our knowledge, suggesting convergence of behavioral, epigenetic, and neuroimaging data that form a psychobiological signature of parenting-risk in the context of early life stress and PTSD.

Cortical control of facial expression.

The present topical review deals with the motor control of facial expressions in humans. Facial expressions are a central part of human communication. Emotional face expressions have a crucial role in human non-verbal behavior, allowing a rapid transfer of information between individuals. Facial expressions can be both voluntarily or emotionally controlled. Recent studies in non-human primates and humans revealed that the motor control of facial expressions has a distributed neural representation. At least 5 cortical regions on the medial and lateral aspects of each hemisphere are involved: the primary motor cortex, the ventral lateral premotor cortex, the supplementary motor area on the medial wall, and, finally, the rostral and caudal cingulate cortex. The results of studies in humans and non-human primates suggest that the innervation of the face is bilaterally controlled for the upper part, and mainly contralaterally controlled for the lower part. Furthermore, the primary motor cortex, the ventral lateral premotor cortex, and the supplementary motor area are essential for the voluntary control of facial expressions. In contrast, the cingulate cortical areas are important for emotional expression, since they receive input from different structures of the limbic system. This article is protected by copyright. All rights reserved.

Evaluation of scleral and corneal thickness in keratoconus patients

PURPOSE To determine whether the scleral stroma is affected as much as the corneal stroma in keratoconus. SETTING University Eye Clinic, Bern, Switzerland. DESIGN Comparative case-control study. METHODS Eyes with keratoconus (keratoconus group) and eyes of age-, sex-, and axial length-matched controls (control group) were analyzed. Corneal videokeratometry and pachymetry were performed using a Scheimpflug tomographer (Pentacam). For measurements of the peripheral cornea and the anterior sclera, a spectral-domain anterior segment optical coherence tomography device (Spectralis) was used. RESULTS The study group comprised 51 eyes and the control group, 50 eyes. The mean central corneal thickness in the keratoconus group was statistically significantly lower than in the control group (447.8 μm ± 57.8 [SD] versus 550.5 ± 35.5 μm) (P < .0001). No significant difference in the mean anterior scleral thickness was found between the keratoconus group and the control group (479.1 ± 43.7 μm versus 474.2 ± 43.0 μm) (P =.57). CONCLUSION Although corneal thinning was observed in keratoconus patients, the anterior scleral stroma thickness in these patients seemed to be similar to that in healthy control eyes.

Distinct roles of cortical and pallidal β and γ frequencies in hemiparkinsonian and dyskinetic rats.

Enhanced β band (βB) activity, which is suppressed by levodopa (LD) treatment, has been demonstrated within the basal ganglia (BG) of Parkinson's disease (PD) patients. However, some data suggest that Parkinsonian symptoms are not directly related to this brain frequency and therefore, its causative role remains questionable. A less explored phenomenon is the link between the γ band (γB) and PD phenomenology. Here, we monitored the development of the oscillatory activity during chronic LD depletion and LD treatment in Parkinsonian and levodopa-induced dyskinesia (LID) in rats. We found a significant and bilateral power increase in the high βB frequencies (20-30Hz) within the first 10days after 6-hydroxydopamine (6-OHDA) lesion, which was in accordance with a significant depletion of dopaminergic fibers in the striatum. We also observed a clear-cut γB increase during LD treatment. The development of LID was characterized by a slight increase in the cumulative power of βB accompanied by a large augmentation in the γB frequency (60-80Hz). This latter effect reached a plateau in the frontal cortex bilaterally and the left globus pallidus after the second week of LD treatment. Our data suggest that the βB parallels the emergence of Parkinsonian signs and can be taken as a predictive sign of DA depletion, matching TH-staining reduction. On the other hand, the γB is strictly correlated to the development of LID. LD treatment had an opposite effect on βB and γB, respectively.

Cervical spinal locking plate in combination with cortical ring allograft for a one level fusion in dogs with cervical spondylotic myelopathy.

OBJECTIVE To evaluate use of a surgical technique commonly used in humans for treatment of cervical spondylotic myelopathy (CSM) in dogs. DESIGN Prospective case series. ANIMALS Dogs with CSM (n=10). METHODS Dogs weighing >30 kg that had CSM at 1 vertebral articulation were eligible for inclusion. Dogs had vertebral column distraction/fusion performed using a cortical ring allograft, cancellous autograft, and a spinal locking plate. Dogs were evaluated temporally by repeat neurological examinations and by client perception of postsurgical outcome, determined by telephone interview. RESULTS Nine dogs survived the immediate postoperative period. Seven of 8 dogs had moderate to complete improvement without recurrence (mean follow-up, 2.48 years). The most common postsurgical complications were screw loosening (n=4) and plate shifting (2), neither of which required surgical revision. One dog had pseudoarthrosis that may have negatively impacted outcome. CONCLUSION Treatment of single level CSM in dogs with ring allograft and a spinal locking plate system may lead to successful outcomes. The major problems encountered with included cost of the implants and adjusting the system designed for humans to fit the vertebral column of a dog. CLINICAL RELEVANCE For dogs with CSM at a single level, the use of a spinal locking plate in combination with a cortical ring allograft can be an effective surgical treatment. Costs of the implants as well as anatomic differences in dogs make this type of surgery less appealing.

Streptococcus pneumoniae capsule determines disease severity in experimental pneumococcal meningitis.

Streptococcus pneumoniaebacteria can be characterized into over 90 serotypes according to the composition of their polysaccharide capsules. Some serotypes are common in nasopharyngeal carriage whereas others are associated with invasive disease, but when carriage serotypes do invade disease is often particularly severe. It is unknown whether disease severity is due directly to the capsule type or to other virulence factors. Here, we used a clinical pneumococcal isolate and its capsule-switch mutants to determine the effect of capsule, in isolation from the genetic background, on severity of meningitis in an infant rat model. We found that possession of a capsule was essential for causing meningitis. Serotype 6B caused significantly more mortality than 7F and this correlated with increased capsule thickness in the cerebrospinal fluid (CSF), a stronger inflammatory cytokine response in the CSF and ultimately more cortical brain damage. We conclude that capsule type has a direct effect on meningitis severity. This is an important consideration in the current era of vaccination targeting a subset of capsule types that causes serotype replacement.

Transcranial magnetic stimulation (TMS) inhibits cortical dendrites

One of the leading approaches to non-invasively treat a variety of brain disorders is transcranial magnetic stimulation (TMS). However, despite its clinical prevalence, very little is known about the action of TMS at the cellular level let alone what effect it might have at the subcellular level (e.g. dendrites). Here, we examine the effect of single-pulse TMS on dendritic activity in layer 5 pyramidal neurons of the somatosensory cortex using an optical fiber imaging approach. We find that TMS causes GABAB-mediated inhibition of sensory-evoked dendritic Ca(2+) activity. We conclude that TMS directly activates fibers within the upper cortical layers that leads to the activation of dendrite-targeting inhibitory neurons which in turn suppress dendritic Ca(2+) activity. This result implies a specificity of TMS at the dendritic level that could in principle be exploited for investigating these structures non-invasively.